We have found that some RNA polymerase mutants of E. coli obtained by rifampicin resistance poorly support the growth of the bacterial virus T4. T2, T6, and beta glucosyl transeferaseless (beta gt minus) mutants of T4 grow much better than wild type T4. We are analyzing the effects of the RNA polymerase mutations on different functions in phage development and the effects of beta gt mutants on each of these functions. The RNA polymerase mutations delay most nucleoid unfolding and the degradation of host DNA as well as delaying the shutoff of host transcription. They also cause a delay in T4 DNA replication and a severe defect in late gene expression. T4beta gt mutations affect the defect in late gene expression and the delay in host DNA breakdown but not the delay in nucleoid unfolding or the delay in shutoff of host transcription. We are looking for changes which do not occur to the RNA polymerase after infection of the mutant cells. We are also investigating the cellular distribution of beta glucose on T4 DNA during infection.